Proprioceptive Deafferentation Research Articles

Force sense deficits in chronic ankle instability: A systematic review and meta-analysis.

Patients with chronic ankle instability (CAI) may experience ankle force sense deficits due to mechanoreceptor injury and proprioceptive deafferentation in the affected ankles. This study aimed to systematically review the literature and investigate (1) whether patients with CAI have impaired force sense when compared with uninjured contralateral sides or healthy controls, and (2) which characteristics of CAI (e.g., any measurement of CAI symptoms, clinical questionnaires, or functional tests on the injured ankles) are correlated with force sense deficits. TYPE: Systematic review and meta-analysis. PubMed, Embase, Web of Science, Cochrane Library, Scopus, CINAHL, and SPORTDiscus were searched for ankle-related, injury-related, and force sense-related terms from inception to February 2, 2022. The following information was extracted from included articles: demographic data, sample size, selection criteria, methodology, force reproduction test outcomes, and correlations between force sense and other characteristics of CAI. Meta-analyses were conducted for the force sense outcomes, and a narrative review was undertaken for the correlation between force sense deficits and other characteristics of CAI. Eight studies were included. The meta-analyses revealed eversion force sense deficits of the injured ankles in absolute error (magnitude of force reproduction error) at 20% maximal voluntary isometric contractions (MVIC) (standardized mean difference [SMD]=0.67, 95% confidence interval [CI] 0.23-1.11) and variable error (consistency of force reproduction) at 30% MVIC (SMD=0.46, 95% CI 0.07-0.85), as compared with healthy controls. None of the included studies reported a significant correlation between these two deficits and other characteristics of CAI. Patients with CAI have eversion force sense deficits in the magnitude of force reproduction error at 20% MVIC and the consistency of force reproduction at 30% MVIC.

Reversible pseudoathetosis and sensory ataxic gait caused by cervical spondylotic myelopathy

Proprioceptive deafferentation of spinal cord origin can cause pseudoathetosis, sensory ataxic gait, or both. The co-existence of pseudoathetosis and sensory ataxic gait caused by a surgically treatable condition of the spinal cord has been rarely reported. An 80-year-old man with cervical spondylotic myelopathy presented with severe sensory ataxic gait which confined him to a wheelchair. He also had poor control of his hands due to the pseudoathetoid movements of the fingers, which prevented him from sustaining constant muscle contraction. He underwent C3-4 and C4-5 anterior discectomies and anterior fusion. His neurological deficits gradually improved after the decompressive surgery. About 7months postoperatively, he was totally independent in activities of daily living and needed no mobility aid. This case highlights the clinical importance of recognizing a surgically treatable and reversible condition of the spinal cord that causes pseudoathetosis and sensory ataxic gait.

Proprioceptive deafferentation slows down the processing of visual hand feedback

During visually guided movements both vision and proprioception inform the brain about the position of the hand, so interaction between these two modalities is presumed. Current theories suggest that this interaction occurs by sensory information from both sources being fused into a more reliable, multimodal, percept of hand location. In the literature on perception, however, there is evidence that different sensory modalities interact in the allocation of attention, so that a stimulus in one modality facilitates the processing of a stimulus in a different modality. We investigated whether proprioception facilitates the processing of visual information during motor control. Subjects used a computer mouse to move a cursor to a screen target. In 28% of the trials, pseudorandomly, the cursor was rotated or the target jumped. Reaction time for the trajectory correction in response to this perturbation was compared under conditions with normal and reduced proprioception after 1-Hz rTMS over the hand-contralateral somatosensory cortex. Proprioceptive deafferentation slowed down the reaction time for initiating a motor correction in response to a visual perturbation in hand position, but not to a target jump. Correlation analyses suggested that reaction time was influenced by the size of the visual error rather than the visuo-proprioceptive conflict or the variance in cursor position. We suggest that during movements intact proprioception is necessary for the rapid processing of visual feedback.

Enhanced Accuracy in Novel Mirror Drawing after Repetitive Transcranial Magnetic Stimulation-Induced Proprioceptive Deafferentation

When performing visually guided actions under conditions of perturbed visual feedback, e.g., in a mirror or a video camera, there is a spatial conflict between visual and proprioceptive information. Recent studies have shown that subjects without proprioception avoid this conflict and show a performance benefit. In this study, we tested whether deafferentation induced by repetitive transcranial magnetic stimulation (rTMS) can improve mirror tracing skills in normal subjects. Hand trajectory error during novel mirror drawing was compared across two groups of subjects that received either 1 Hz rTMS over the somatosensory cortex contralateral to the hand or sham stimulation. Mirror tracing was more accurate after rTMS than after sham stimulation. Using a position-matching task, we confirmed that rTMS reduced proprioceptive acuity and that this reduction was largest when the coil was placed at an anterior parietal site. It is thus possible, with rTMS, to enhance motor performance in tasks involving a visuoproprioceptive conflict, presumably by reducing the excitability of somatosensory cortical areas that contribute to the sense of hand position.

Mouvements choréo-athétosiques et syndrome anti-Hu

Paraneoplastic choreo-athetoses are rare. We report a case of anti-Hu syndrome with choreo-athetosis. A 48-year-old woman developed a small-cell lung carcinoma revealed by an anti-Hu syndrome. The neurological features included choreo-athetosis predominating in the upper limbs, chronic sensorimotor axonal polyneuropathy, and opsoclonus. The cerebrospinal fluid was acellular and contained several oligoclonal IgG bands, not found in the corresponding serum. Magnetic resonance imaging revealed bilateral high-intensity lesions on T2/FLAIR sequence in the corona radiata. Moderate transitory improvement of the paraneoplastic neurological syndrome was observed after several carboplatin-etoposid cycles. A paraneoplastic origin must be considered in all cases of unexplained choreo-athetosis. Paraneoplastic choreo-athetosis is most often associated with other neurological symptoms. The most frequent associated tumor is a small-cell lung carcinoma with anti-CRMP5 and/or anti-Hu antibodies. Our patient developed paraneoplastic choreo-athetosis related to an anti-Hu syndrome in the absence of anti-CRMP5/CV2 antibodies. Paraneoplastic choreo-athetosis might result from a central lesion, and/or from proprioceptive deafferentation subsequent to peripheral neuropathy.

Oculomotor function in the rhesus monkey after deafferentation of the extraocular muscles.

The function of extraocular muscle proprioception in the control of eye movements remains uncertain. In this study, we examined the effect of bilateral proprioceptive deafferentation of the extraocular muscles on eye movements in two rhesus monkeys. Before and after deafferentation, we analyzed baseline ocular alignment, saccades, pursuit, and vestibular eye movements. We also examined visually mediated adaptation of ocular alignment, saccades, and pursuit. Deafferentation of the eye muscles did not affect baseline ocular motor control, either acutely or over a 5-week period of study. Furthermore, visually mediated adaptation of the eye movement subtypes was also unaffected by deafferentation. These results suggest that ocular proprioception in primates is not used in the immediate, on-line control of eye movements and does not interact with visual cues in the adaptive modification of ocular motor function. We conclude that the efferent command (efference copy) provides sufficient information about eye kinematics to the brain for accurate eye movement control in normal monkeys, and that this information is modified by visual feedback independently of proprioception. We hypothesize that proprioception may be used to calibrate the efference copy during development and in response to perturbations by signaling potential mismatches between eye movement information derived from the efferent command and the actual motion of the eye transduced by the proprioceptive organs.

Proprioceptive and retinal afference modify postsaccadic ocular drift.

Drift of the eyes after saccades produces motion of images on the retina (retinal slip) that degrades visual acuity. In this study, we examined the contributions of proprioceptive and retinal afference to the suppression of postsaccadic drift induced by a unilateral ocular muscle paresis. Eye movements were recorded in three rhesus monkeys with a unilateral weakness of one vertical extraocular muscle before and after proprioceptive deafferentation of the paretic eye. Postsaccadic drift was examined in four visual states: monocular viewing with the normal eye (4-wk period); binocular viewing (2-wk period); binocular viewing with a disparity-reducing prism (2-wk period); and monocular viewing with the paretic eye (2-wk period). The muscle paresis produced vertical postsaccadic drift in the paretic eye, and this drift was suppressed in the binocular viewing condition even when the animals could not fuse. When the animals viewed binocularly with a disparity-reducing prism, the drift in the paretic eye was suppressed in two monkeys (with superior oblique pareses) but generally was enhanced in one animal (with a tenotomy of the inferior rectus). When drift movements were enhanced, they reduced the retinal disparity that was present at the end of the saccade. In the paretic-eye-viewing condition, postsaccadic drift was suppressed in the paretic eye and was induced in the normal eye. After deafferentation in the normal-eye-viewing state, there was a change in the vertical postsaccadic drift of the paretic eye. This change in drift was idiosyncratic and variably affected the amplitude and velocity of the postsaccadic drift movements of the paretic eye. Deafferentation of the paretic eye did not affect the postsaccadic drift of the normal eye nor did it impair visually mediated adaptation of postsaccadic drift. The results demonstrate several new findings concerning the roles of visual and proprioceptive afference in the control of postsaccadic drift: disconjugate adaptation of postsaccadic drift does not require binocular fusion; slow, postsaccadic drift movements that reduce retinal disparity but concurrently increase retinal slip can be induced in the binocular viewing state; postsaccadic drift is modified by proprioception from the extraocular muscles, but these modifications do not serve to minimize retinal slip or to correct errors in saccade amplitude; and visually mediated adaptation of postsaccadic drift does not require proprioceptive afference from the paretic eye.

Efference copy provides the eye position information required for visually guided reaching.

The contribution of extraocular muscle (EOM) proprioception to the eye position signal used to transform retinotopic visual information to a craniotopic reference frame remains uncertain. In this study we examined the effects of unilateral and bilateral proprioceptive deafferentation of the EOMs on the accuracy of reaching movements directed to visual targets. No significant changes occurred in the mean accuracy (constant error) or variance (variable error) of pointing after unilateral or bilateral deafferentation. We concluded that in normal animals efference copy provides sufficient information about orbital eye position to code space in craniotopic coordinates.

Extraocular muscle proprioception functions in the control of ocular alignment and eye movement conjugacy.

1. The function of extraocular muscle proprioception in the control of eye movements is uncertain. We tested the hypothesis that proprioception contributes to the long-term regulation of ocular alignment and eye movement conjugacy. 2. Eye movements were recorded in monkeys with unilateral extraocular muscle palsies, before and after proprioceptive deafferentation of the paretic eye. Following deafferentation, ocular alignment and saccade conjugacy gradually worsened over several weeks. In contrast, disconjugate adaptation induced by habitual binocular viewing with a prism (disparity-mediated adaptation) occurred normally after deafferentation. 3. These results provide the first evidence that proprioception functions in the control of eye movements in primates, and indicate that proprioception contributes to the long-term adaptive mechanisms that regulate ocular alignment during fixation and saccades. The error signal used in this process may be derived from a mismatch between the efference copy and proprioceptive afference.

Long-term dysfunctions of neural stereoscopic mechanisms after unilateral extraocular muscle proprioceptive deafferentation.

1. Neural correlates of the permanent deficits in depth perception that occur when extraocular muscle proprioceptive (EMP) afferents are interrupted unilaterally in kittens were investigated by performing extracellular recordings in the primary visual cortex (area 17) in adulthood. Unilateral section of the ophthalmic branch of the trigeminal nerve (V1 nerve) were performed in 11 cats when they were between 5 and 12 weeks of age (uni-V1 group). Electrophysiological results were compared with those obtained in 17 normal adult cats (control group). 2. Binocular interactions were assessed by testing the sensitivity of cortical neurons to dichoptic presentations of moving sine-wave gratings whose interocular positional phase relationship was randomly varied. The amplitude modulation between the minimum and the maximum binocular responses defined the dynamic range. The degree of binocular suppression or facilitation was assessed by comparing these binocular response limits with the optimal monocular responses evoked through either eye at the best spatial frequency. The variability of both monocular and binocular responses was estimated by using the variation coefficient. 3. In uni-V1 cats, both the dynamic range and the degree of binocular suppression were significantly less pronounced than in controls, whereas binocular facilitation was not affected. The variability of the binocular responses was significantly increased, unlike monocular responses, whose variability was similar to control values. 4. From Fourier analysis of the poststimulus time histograms, two clear-cut categories of cells emerged that were differentially affected in the uni-V1 group. The "modulated" cells showed significantly less binocular suppression than in controls, and the "unmodulated" cells had binocular responses that were significantly more variable than in controls. Results from "simple" cells were similar to those of modulated cells, and results from "complex" cells were similar to those of unmodulated cells. However, in the unmodulated population, which was composed of both simple and complex cells, it was shown that the increase of variability was due to that of complex cells. 5. A nonparametric statistical test was applied on the interocular phase shift tuning curves to determine the minimum stimulus change necessary to elicit a significant change in the neural response. Two categories of cells were determined: the "discriminative" cells (80% in controls but 45% in uni-V1 cats) combined pronounced binocular suppression and dynamic range with relatively low variability. The reverse was true in the case of "nondiscriminative" cells (20% in controls and 55% in uni-V1 cats). 6. In uni-V1 cats, about half of the cells were monocularly activated.(ABSTRACT TRUNCATED AT 400 WORDS)

The period of susceptibility of visual cortical binocularity to unilateral proprioceptive deafferentation of extraocular muscles.

1. The electrophysiological effects of section of extraocular muscle proprioceptive afferents have been investigated in kitten area 17. Extraocular proprioceptive afferents were interrupted by cutting the ophthalmic branch of the fifth trigeminal nerve (V1 nerve) unilaterally in 15 normally reared kittens (NR) between 3 and 12 wk postnatal, in 3 NR adult cats, and in 7 dark-reared (DR) kittens at 6 wk postnatal. Bilateral sections of the V1 nerve were performed in two kittens at 6 wk postnatal. NR kittens were maintained in a normal environment after the section. DR kittens were returned to the darkroom until the recording session. Receptive-field properties of area 17 neurons were studied after a postsurgical delay of 4-7 wk in most NR kittens and of 4 days to 5 wk in DR kittens. In one NR kitten and in the operated adult cats, the delay was 1-2.5 yr. This study is based on a total sample of 1,190 visual cortical units. 2. When performed in NR kittens between 4 and 8 wk of age, the unilateral section of extraocular proprioceptive afferents significantly reduced the proportion of binocular cells: 1 mo after the section of the V1 nerve, half of the visual cortical cells were monocularly activated. A similar reduction in the proportion of binocular cells was also observed in DR kittens operated at 6 wk of age and then maintained in the dark for 5-7 wk. In contrast to the unilateral section, the bilateral section of the V1 nerve performed in 6-wk-old NR kittens did not disrupt cortical binocularity. 3. In 10 of the 22 kittens that had undergone unilateral sections, there was a strong asymmetry in the ocular dominance distribution in favor of one eye. This asymmetry was not related to the side of the section and was the same in both hemispheres for a given kitten. 4. The postsurgical delay played an important role in the appearance of the cortical deficit: binocularity loss was not found within the week following the section but was present 1 mo after the section. This functional impairment appeared to be permanent, since it was still observed 2.5 yr after the section. 5. Cortical cells were classified in two ways on the basis of their receptive-field organization: 1) into S- or C-types (38, 73), and 2) into small area slow (SAS), large area slow (LAS), or Fast (F)-types (42, 57).(ABSTRACT TRUNCATED AT 400 WORDS)

Impairment of stereoacuity in cats with oculomotor proprioceptive deafferentation

Impairment of stereoacuity in cats with oculomotor proprioceptive deafferentation

Impairment of stereoacuity in cats with oculomotor proprioceptive deafferentation.

Stereoacuity was measured with an operant conditioning technique in adult cats with unilateral deafferentation of oculomotor proprioception (section of the ophthalmic branch of the fifth cranial nerve). Binocular stereoacuity was found not to exceed monocular depth sensitivity, in contrast to what is obtained in normal cats. The results confirm previous findings and indicate a role of oculomotor proprioception in binocular depth perception of the cat.

Deafferentation of oculomotor proprioception affects depth discrimination in adult cats.

Depth discrimination was tested behaviourally in adult cats prior to and after chronic section of the ophthalmic branch of the Vth cranial nerve, that contains the majority of oculomotor proprioceptive fibers. Binocular depth discrimination was considerably impaired following either unilateral or bilateral oculomotor proprioceptive deafferentation.

Unusual presentation of Charcot-Marie-Tooth disease — Incoordination with absent or minimal wasting: Report of 2 cases

Two patients are reported presenting with incoordination mimicking cerebellar disease in the upper and lower limbs, ataxia of gait, absent tendon reflexes and little or no clinically detectable wasting. Motor conduction velocity in the upper limbs was substantially reduced in one patient whereas it was normal and slightly reduced in the other. It is concluded that in Charcot-Marie-Tooth disease incoordination may mimic cerebellar disease and when this is so it is due to the association of varying degrees of proprioceptive deafferentation and a dyskinesia similar to that produced by familial (essential) tremor.